Volatile Organic Compound Gamma-Butyrolactone Released upon Herpes Simplex Virus Type -1 Acute Infection Modulated Membrane Potential and Repressed Viral Infection in Human Neuron-Like Cells
Fig 8
Proposed model of latency establishment by GBL.
The working hypothesis is that GBL production is induced upon HSV-1 primary infection and this modulated the membrane potential of sensory neurons adjacent to the infected epithelial cells. This event can potentially alter the signaling pathway within the neurons, inhibiting viral gene expression and replication, thereby promoting latency establishment.